Heart disease, specifically coronary artery disease, is a major cause of death, disability, and healthcare expense in the United States and other industrialized countries. Until recently, most heart disease was considered the result of a progressive increase of hard plaque in the coronary arteries. The commonly held theory postulated that an atherosclerotic disease process of hard plaques led to a critical narrowing (stenosis) of the affected coronary artery to produce anginal syndromes, commonly known as chest pain. The progression of the arterial narrowing reduced blood flow, triggering blood clot formation. The blood clot might choke off the flow of oxygen rich blood (ischemia) to heart muscles, causing a heart attack, or alternatively, the blood clot might break from the vessel wall and lodge in another organ vessel, such as the brain, causing a thrombotic stroke.
Within the past decade, evidence has emerged challenging this model of atherosclerosis, coronary artery disease, and heart attacks. While the build up of hard plaque may produce angina and severe ischemia in the coronary arteries, new clinical data now suggests that the rupture of sometimes non-occlusive, vulnerable plaques causes the vast majority of heart attacks. The rate of heart attacks due to vulnerable plaques is estimated as high as 60 to 80 percent. In many instances vulnerable plaques do not impinge on the vessel lumen, but are like an abscess ingrained beneath the arterial wall. For this reason, conventional angiography or fluoroscopy techniques that indicate vessel flow area are unlikely to detect the vulnerable plaque. Due to the difficulty of detection and lack of symptoms such as angina, vulnerable plaques may be more dangerous than other plaques that cause pain. Currently, no strategy exists for reliably identifying vulnerable plaques.
Formation and rupture of vulnerable plaques can result in heart attack and/or stroke. The majority of vulnerable plaques include a lipid pool, smooth muscle (endothelial) cells, and a dense infiltrate of macrophages, all contained by a thin fibrous cap. The lipid pool is believed to form because of pathological processes involving low density lipoprotein (LDL), macrophages, and the inflammatory process. The macrophages oxidize the LDL producing foam cells. The macrophages, foam cells, and associated endothelial cells release various substances, such as tumor necrosis factor, tissue factor, and matrix proteinases, which result in generalized cell necrosis and apoptosis, pro-coagulation, and weakening of the fibrous cap. The inflammation process may weaken the fibrous cap to the extent that mechanical stress, such as that produced by increased blood pressure, may result in rupture. The lipid core and other contents of the vulnerable plaque may then spill into the blood stream thereby initiating a clotting cascade. The cascade produces a blood clot (thrombosis) that potentially results in a heart attack and/or stroke. The process is exacerbated due to the release of collagen and plaque components, e.g., collagen and tissue factor, which enhance clotting upon their release.
Balloon catheters are used in a variety of medical therapeutic applications including intravascular angioplasty. For example, a balloon catheter device is inflated during PTCA (percutaneous transluminal coronary angioplasty) to dilate a stenotic blood vessel. After inflation, the pressurized balloon exerts a compressive force on the lesion thereby increasing the inner diameter of the affected vessel. Some exemplary balloon catheters are disclosed in U.S. Pat. No. 4,490,421 to Levy, U.S. Pat. No. 5,451,233 to Yock, and U.S. Pat. No. 4,762,129 to Bonzel, incorporated herein by reference.
Vulnerable plaque typically is detected by sensing elevated temperature in the vulnerable plaque relative to the surrounding tissue. The elevated temperature results from the inflammation of and the increased metabolic activity in the vulnerable plaque. The temperature increase may be from a fraction of a degree to a few degrees Celsius, e.g., from 0.1–0.2 degrees Celsius to 1.25–1.65 degrees Celsius. Existing temperature sensing systems use pinpoint sized temperature sensors with a small surface area, which only sense a very small area of the vessel wall tissue and may easily overlook vulnerable plaque lesions. While these sensors may be adequate to detect vulnerable plaque when the sensors actually touch the vulnerable plaque, they typically miss a large portion of the arterial wall. Reliable detection of a vulnerable plaque lesion is not assured.
Existing temperature sensing systems have additional limitations. Typical sensors such as thermisters are discrete units fastened to a catheter or balloon. Such sensors are expensive and cost may limit the number of sensors that are used, limiting the resolution of the temperature mapping: current practice is to disregard the circumferential temperature variation and concentrate on the longitudinal variation to reduce the number of sensors. This may miss a vulnerable plaque localized to a partial circumference of the vessel. Use of discrete thermal sensors also results in the need to bring one or more wires from each thermal sensor to the outside of the patient during testing. This increases the size of the catheter lead and fabrication expenses.
U.S. Pat. No. 5,871,449 to Brown discloses a system for locating inflamed plaque including a catheter with an expander, the expander being operable to move a carrier transmitting infrared radiation into contact with the arterial wall.
U.S. Pat. No. 5,924,997 to Campbell discloses an intravascular catheter system capable of mapping thermal variations in the temperature of athrosclerotic plaque, incorporating a plurality of thermal sensors fixedly attached along the catheter's multi-lumen flexible tubular member.
U.S. Pat. No. 6,245,026 to Campbell et al. discloses a variety of thermal mapping catheters capable of sensing and mapping thermal variations in body vessels, in vascular applications the catheters being capable of detecting temperature variations in athrosclerotic plaque.
U.S. Patent application publication Ser. No. US 2001/0047138 to Kokate et al. discloses a method and device for detecting vulnerable plaque including an elongate shaft, a substrate fixed to the elongate shaft, and a plurality of sensors disposed on the substrate.
U.S. Patent application publication Ser. No. US 2002/0082515 to Campbell et al. discloses interventional tools suitable for measuring the temperature or temperature variations in a vessel wall and thereafter treating vulnerable plaque that is identified during the thermal mapping.
It would be desirable to have a temperature mapping balloon that would overcome the above disadvantages.